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Control of G1 arrest after DNA damage.

Publication ,  Journal Article
Kastan, MB; Kuerbitz, SJ
Published in: Environ Health Perspect
December 1993

The temporal relationship between DNA damage and DNA replication may be critical in determining whether the genetic changes necessary for cellular transformation occur after DNA damage. Recent characterization of the mechanisms responsible for alterations in cell-cycle progression after DNA damage in our laboratory have implicated the p53 (tumor suppressor) protein in the G1 arrest that occurs after certain types of DNA damage. In particular, we found that levels of p53 protein increased rapidly and transiently after nonlethal doses of gamma irradiation (XRT) in hematopoietic cells with wild-type, but not mutant, p53 genes. These changes in p53 protein levels were temporally linked to a transient G1 arrest in these cells. Hematopoietic cells with mutant or absent p53 genes did not exhibit this G1 arrest, through they continued to demonstrate a G2 arrest. We recently extended these observations of a tight correlation between the status of the endogenous p53 genes and this G1 arrest after XRT and this cell-cycle alteration after XRT was then established by transfecting cells lacking endogenous p53 genes with a wild-type gene and observing acquisition of the G1 arrest and by transfecting cells processing endogenous wild-type p53 genes with a mutant p53 gene and observing loss of the G1 arrest after XRT. These observations and their significance for our understanding of the mechanisms of DNA damage-induced cellular transformation are discussed.

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Published In

Environ Health Perspect

DOI

ISSN

0091-6765

Publication Date

December 1993

Volume

101 Suppl 5

Issue

Suppl 5

Start / End Page

55 / 58

Location

United States

Related Subject Headings

  • Toxicology
  • Mutation
  • Humans
  • Genes, p53
  • Gamma Rays
  • G1 Phase
  • DNA Replication
  • DNA Damage
  • Animals
  • 42 Health sciences
 

Citation

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Kastan, M. B., & Kuerbitz, S. J. (1993). Control of G1 arrest after DNA damage. Environ Health Perspect, 101 Suppl 5(Suppl 5), 55–58. https://doi.org/10.1289/ehp.93101s555
Kastan, M. B., and S. J. Kuerbitz. “Control of G1 arrest after DNA damage.Environ Health Perspect 101 Suppl 5, no. Suppl 5 (December 1993): 55–58. https://doi.org/10.1289/ehp.93101s555.
Kastan MB, Kuerbitz SJ. Control of G1 arrest after DNA damage. Environ Health Perspect. 1993 Dec;101 Suppl 5(Suppl 5):55–8.
Kastan, M. B., and S. J. Kuerbitz. “Control of G1 arrest after DNA damage.Environ Health Perspect, vol. 101 Suppl 5, no. Suppl 5, Dec. 1993, pp. 55–58. Pubmed, doi:10.1289/ehp.93101s555.
Kastan MB, Kuerbitz SJ. Control of G1 arrest after DNA damage. Environ Health Perspect. 1993 Dec;101 Suppl 5(Suppl 5):55–58.

Published In

Environ Health Perspect

DOI

ISSN

0091-6765

Publication Date

December 1993

Volume

101 Suppl 5

Issue

Suppl 5

Start / End Page

55 / 58

Location

United States

Related Subject Headings

  • Toxicology
  • Mutation
  • Humans
  • Genes, p53
  • Gamma Rays
  • G1 Phase
  • DNA Replication
  • DNA Damage
  • Animals
  • 42 Health sciences